〔Abstract〕 Objective To investigate the protective effect of wogonin on acute kidney injury(AKI) induced by lipopolysaccharide(LPS). Methods The model of septic-induced AKI was established on male C57BL/6J mice by a single intraperitoneal injection of LPS and normal C57BL/6J mice were used as normal control group. Twenty-four male C57BL/6 mice were randomly divided into 4 groups(6 mice in each group): normal control group(NC), normal control+wogonin(NC+WOG 12.5 mg/kg), LPS model group(LPS 10 mg/kg), LPS model+wogonin(LPS 10 mg/kg+WOG 12.5 mg/kg). After LPS intervention for 24 h, serum samples were collected to detect blood creatinine(CRE) and urea nitrogen(BUN) levels. HE staining and PAS staining were performed to observe the degree of renal pathological injury. Immunohistochemistry was performed to detect the degree of expression of inflammatory markers interleukin(IL)-1β, IL-6 and tumor necrosis factor(TNF)-α in renal tissues. PCR was performed to detect the expression of KIM-1 and NGAL in renal tissues. Western blot was performed to detect the changes in protein expression of NF-κB signaling pathway subunits P65 and PP65 in renal tissues. Results Compared with NC group, CRE and BUN levels in LPS group increased(FCRE=60.90,P<0.001,FBUN=82.13,P<0.001); compared with LPS group, these indexes decreased in LPS+WOG group(P<0.001). PCR test results showed that compared with the NC group, the expression ofKIM-1andNGALmRNA was significantly increased in LPS group(FKIM-1=146.3,P<0.001,FNGAL=161.2,P<0.001). In contrast,KIM-1andNGALmRNA expression was decreased in the LPS+WOG group(P<0.01). Renal histopathological examination showed that compared with the NC group, renal tissues of mice had renal tubular dilatation and inflammatory cell infiltration in LPS group; compared with LPS group, the number of tubular dilatation reduced and inflammatory cell infiltration was reduced in LPS+WOG group(FHE=721.4,P<0.001;FPAS=518.9,P<0.001). Immunohistochemical staining showed that the expression of IL-1β, IL-6 and TNF-α was significantly increased in the LPS group; compared with the LPS groups(FIL-1β=114.6,FIL-6=108.9,FTNF-α=251.6, allP<0.001), these indexes decreased in LPS+WOG group(allP<0.01). Further studies using Western blot showed that the NF-κB signaling pathway of LPS-treated mice had been activated and produced a hyperphosphorylated state in comparison to the NC group(FPP65=13.02,P<0.01), yet this pathway in the LPS+WOG group showed the opposite effect, namely attenuated activity and reduced phosphorylation when the control was LPS(P<0.01). Conclusion WOG effectively blocked the NF-κB signaling pathway in the LPS-induced acute kidney injury model mice, thereby attenuating the inflammatory response and tissue damage in the kidneys of LPS-induced acute kidney injury mice.